| Autor: |
Batra Raj K, Huang Min, Zhu Li X, Hillinger Sven, Yang Seok-Chul, Sharma Sherven, Lin Jeff F, Burdick Marie D, Strieter Robert M, Dubinett Steven M |
| Jazyk: |
angličtina |
| Rok vydání: |
2003 |
| Předmět: |
|
| Zdroj: |
Molecular Cancer, Vol 2, Iss 1, p 22 (2003) |
| Druh dokumentu: |
article |
| ISSN: |
1476-4598 |
| DOI: |
10.1186/1476-4598-2-22 |
| Popis: |
Abstract Background SLC/CCL21, normally expressed in high endothelial venules and in T cell zones of spleen and lymph nodes, strongly attracts T cells and dendritic cells (DC). We have previously shown that SLC/CCL21-mediated anti-tumor responses are accompanied by significant induction of IFNγ and the CXC chemokines, monokine induced by IFNγ (MIG/CXCL9) and IFNγ-inducible protein-10 (IP-10/CXCL10). Results We assessed the importance of IFNγ, IP-10/CXCL10 and MIG/CXCL9 in SLC/CCL21 therapy. In vivo depletion of IP-10/CXCL10, MIG/CXCL9 or IFNγ significantly reduced the anti-tumor efficacy of SLC/CCL21. Assessment of cytokine production at the tumor site showed an interdependence of IFNγ, MIG/CXCL9 and IP-10/CXCL10; neutralization of any one of these cytokines caused a concomitant decrease in all three cytokines. Similarly, neutralization of any one of these cytokines led to a decrease in the frequency of CXCR3+ve T cells and CD11c+ve DC at the tumor site. Conclusion These findings indicate that the full potency of SLC/CCL21-mediated anti-tumor responses require in part the induction of IFNγ, MIG/CXCL9 and IP-10/CXCL10. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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